Variations in assessment and certification in postgraduate anaesthesia training: a European survey.

BACKGROUND: Postgraduate specialty training has traditionally been based on a time- and rotation-based model, but competency-based models are emerging. Because anaesthesia training evolves differently across Europe, variations in assessment and certification processes are expected, but the extent of similarities and differences is unknown. The aim of this study was to compare anaesthesia training programmes in Europe, focusing on assessment and certification processes. METHODS: We performed an online survey among national representatives of the Union of European Medical Specialists/European Board of Anaesthesiology. RESULTS: All 36 countries participated. Duration of training had a median of 5 yr (range 2.75-7). Mean number of different assessment tools was 7.45 (range 4-13), with more tools being used in competency-based programmes [mean 9.1 (sd 2.97) vs 7.0 (sd 1.97); P=0.03]. Most countries had a nationally uniform certification process. Based on a qualitative analysis of the survey findings, a categorization of countries emerged, reflecting the approach to assessment and certification. We observed two main streams of countries with an underlying knowledge or procedural focus within a time- and rotation-based apprenticeship model. These main streams are evolving, to different extents, towards a third orientation, competency-based training. CONCLUSIONS: Assessment and certification processes in European anaesthesia training are diverse. In many countries, a time-based apprenticeship model is evolving towards a competency-based certification process. This diversity precludes comparison of competence of graduating anaesthetists across Europe.

A novel point mutation in cluster 3 of the thyroid hormone receptor beta gene (P247L) causing mild resistance to thyroid hormone.

Resistance to thyroid hormone (RTH), a syndrome characterized by variable tissue hyposensitivity to thyroid hormone (TH), is linked to mutations in the thyroid hormone receptor (TR) beta gene. We report a new family with a heretofore unreported mutation, P247L. The proposita, a 31-year-old female, presented with goiter and palpitations. RTH was suspected because of elevated serum free thyroxine (FT4) level with a normal thyrotropin (TSH). Sequencing the TRbeta gene revealed a mutation causing replacement of a proline at position 247 with leucine. Seven family members were heterozygous for the mutation, two of whom also had evidence of autoimmune thyroid disease. The mutant TRbeta had a Ka for triiodothyronine (T3) 30% that of the wild-type TRbeta, approximately a threefold reduction in T3-induced transactivation and a low level dominant negative activity when tested with a positively regulated reporter gene. In vivo sensitivity to TH was evaluated in three affected subjects by measurement of the responses to graded doses of levotriiodothyronine (LT3). Peak TSH responses to TRH were reduced and were not completely suppressed at even the highest dose of LT3, (0.9, 0.2, and 0.2, compared to < 0.01 microU/mL in unaffected controls), confirming pituitary resistance to TH in all three subjects. In contrast, peripheral tissues responded variably to LT3: serum cholesterol decreased in all by 15%-25%, serum creatine kinase decreased by 15% in two subjects and increased 35% in another, but serum ferritin and sex hormone-binding globulin increased in only one of the three affected individuals that were tested. Basal metabolic rate and sleeping pulse did not change in three and two individuals, respectively. Hyporesponsiveness to exogenous TH established the clinical diagnosis of RTH in one member of the family with a mutant TRbeta but normal tests of thyroid function at baseline. Three affected subjects had an axis I diagnosis of major depression but had Wechsler Intelligence Scale for Children, III (WISC-III) full-scale IQs (FSIQs) in the normal range. This novel TRbeta mutation is associated with a realtively mild RTH. Results of responses to LT3 underscore the variable phenotype of RTH.